Challenges in the study of causation of obesity: Conference on ‘Multidisciplinary approaches to nutritional problems’ Symposium on ‘Diabetes and health’
Open accessAbstract
Use of the energy balance equation for understanding the causation of obesity is discussed. Its basis on the thermodynamic laws is expressed in mathematical models for body-weight changes. Only a very small net energy surplus per time unit constitutes the energy deposition during weight gain, making measurements of its components difficult. The physical laws provide exact quantitative relationships between energy intake, energy expenditure and deposition of energy, but cannot disentangle the initiating and driving forces of the energy imbalance, which may also be an active storage of fat in adipose tissue. These and various other limitations of the energy balance model warrant cautiousness in using the model in studies of obesity causation. Weight gain may be self-promoting and mathematical feedback models allowing estimation of such effects show that they are realistic. Predisposition and susceptibility should be distinguished, and susceptibility as a modifiable predisposition, the genetic and environmental contribution to predisposition and its usefulness as targets for prevention and treatment are discussed. Current progress in unravelling genetic predisposition, the complex genetically-determined mechanisms, the slower progress in unravelling the environmental influences, the different nature of genetic and environmental influences, the possible pathways of environmental influences and the environmental influences as mediators of genetic effects are addressed. The evidence behind the prevailing concept of the ‘obesogenic’ environment is critically analysed. Finally, particular opportunities for the identification of the causes of the obesity epidemic by detailed analysis of an observed irregular development of the epidemic over long time periods are presented, and evidence for predisposition as a result of postnatal environmental influences is inferred from these studies.
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A similar vicious circle is seen for other weight-promoting behaviors, notably physical inactivity and overeating, both of which are reinforced by weight gain.
“Such phenomenon is observed for other weight promoting behaviors, notably physical inactivity and overeating, both of which are reinforced by weight gain [158].”
From Sleep and metabolic function (2012) · cites this paper as [158]
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“Such phenomenon is observed for other weight promoting behaviors, notably physical inactivity and overeating, both of which are reinforced by weight gain [158].”
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- Authors
- Sørensen, T. I. A.
- Affiliations
- University of Copenhagen (DK)
- Corresponding author
- Sørensen, Thorkild I. A.
- Venue
- Proceedings of the Nutrition Society
- Publisher
- Cambridge University Press (CUP)
- Published
- 2008-12-15
- Volume
- 68
- Issue
- 1
- Pages
- 43-54
- ISSN
- 0029-6651 (ISSN-L)
- 1475-2719
- OpenAlex
- W2103742347
- Cited by
- 75
- References
- 53
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 3 · 2023: 3 · 2022: 6 · 2021: 3 · 2020: 2 · 2019: 1 · 2018: 2 · 2017: 1 · 2016: 2 · 2015: 7 · 2014: 8 · 2013: 7 · 2012: 5
- FWCI
- 7.28
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of The Nutrition Society (publishedVersion)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Funders
- Strategiske Forskningsråd (2101-06-0005)
- Topics
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Obesity, Physical Activity, Diet
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- energy balance model, energy intake, energy expenditure, energy deposition, feedback model, genetic susceptibility, environmental influences, obesogenic environment, gene-environment interaction, obesity prevention, obesity epidemic
- MeSH terms
- Adipose Tissue, Adolescent, Basal Metabolism, Energy Intake, Child, Diabetes Mellitus, Diet, Eating, Energy Metabolism, Environment, Female, Homeostasis, Humans, Infant, Low Birth Weight, Infant, Newborn, Male, Models, Theoretical, Obesity, Thermodynamics, Time Factors, Weight Gain, Exercise, Genetic Predisposition to Disease, Young Adult
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